Blocking immune cell signals makes aggressive brain tumor removal easier
Discovery by VIB and KU Leuven researchers points to a potential new treatment strategy.
By Wouter De Smet
••3 min read
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Researchers from VIB and KU Leuven have developed a new strategy to inhibit the spread of glioblastoma, the most aggressive brain tumor, by blocking specific signals between immune cells and tumor cells.
In a new study published in Cancer Cell, researchers from VIB and KU Leuven succeeded in slowing the spread of glioblastoma, the most common and aggressive adult brain tumor, by blocking specific signals between immune cells in the brain and tumor cells. This discovery suggests a potential new treatment strategy: by blocking communication between immune and cancer cells, the tumor remains better delineated and can be removed more easily.
Glioblastoma is the most aggressive brain tumor in adults, with an average survival of about 15 months after diagnosis. The tumor is particularly difficult to treat because tumor cells spread into the surrounding brain tissue, often making complete removal impossible. The more completely a tumor can be removed, the better the patient's survival chances. Finding ways to better delineate the tumor before surgery could therefore be an important strategy to extend patients' lives.
To understand how glioblastoma spread can be counteracted, researchers from the VIB-KU Leuven Center for Cancer Biology, led by prof. Gabriele Bergers, studied the interaction between tumor cells and microglia, the brain's immune cells. Microglia promote glioblastoma development by secreting certain proteins that tumor cells can use to grow. However, the role of lipids, fat-like molecules, in this process was much less known until now.
Using mouse models and tissue from glioblastoma patients, the researchers discovered that tumor cells utilize lipids released by microglia. These lipids make the tumor cells more mobile and help them invade healthy parts of the brain.
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"We discovered that microglia release a specific type of lipid, called lysophosphatidic acids or LPAs. These LPAs then bind to tumor cells and activate processes that help them to spread further through the brain."
Following this initial discovery, the scientists investigated whether they could block this interaction and make the tumor less invasive. This proved to be the case.
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"We were able to interrupt these signals, making the tumors less invasive and better delineated. Although the tumor size did not change, these results point to the possibility of treating patients before surgery, so that their tumor is better delineated and thus easier to remove surgically. Because this approach limits the spread of the tumor but does not shrink the tumor itself, it could be combined with treatments that do shrink the tumor. This could further improve patients' survival chances."
The researchers also checked if they could find the same pattern in human samples. Tests with tumor cells from patients showed that immune cells promoted tumor spread in the same way as in mice.
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"It was quite surprising to see how strongly the mechanism we discovered in mice was also found in human glioblastoma, suggesting that our findings may also be applicable to patients."
The authors emphasize that these are early findings, but the discovery opens the door to a new way of approaching treatment. Professor Gabriele Bergers explains that glioblastomas are very heterogeneous, meaning different parts of the tumor in the same patient can have different mutations. However, their approach targets the communication between immune and cancer cells, not the genetic characteristics of the tumor cells, suggesting it could be applied to a broader range of glioblastomas.
The research was supported by various funds, including the Research Foundation - Flanders (FWO) and Kom op tegen Kanker.
